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PubMed1992

Stone-forming potential of milk or calcium-fortified orange juice in idiopathic hypercalciuric adults.

Milk and orange juice (OJ) fortified with calcium-citrate-malate (CCM; calcium-citrate-malate salt is a coined term to describe a trademarked calcium delivery system found only in Citrus Hill Plus Calcium) were evaluated for their potential to alter urine chemistries and crystallization during the course of an eleven week, crossover study. Six male and six female, non-stone-forming, idiopathic hypercalciuric adults consumed 600 mg per day as beverage calcium for four consecutive weeks. The results show that both milk and CCM-fortified OJ (CCM-OJ) were well tolerated by male and female hypercalciurics since few significant changes occurred in overall urinary chemistry profiles. CCM-OJ did, however, significantly (P less than or equal to 0.05) increase urinary pH relative to milk in both sexes and urinary citrate concentration in women only. Both of these urinary parameters were significantly increased by CCM-OJ in both sexes relative to the basal period. The combined pH and citrate effects are recognized to protect against calcium oxalate stone formation through formation of the soluble calcium citrate salt. These data indicate that either milk or CCM-fortified orange juice can be consumed, at least within the limits tested, as a dietary source of calcium without increasing the risk of stone formation in a calcium-sensitive subpopulation. That the urine chemistries and crystallization of such calcium-sensitive individuals does not significantly change with the consumption of either beverage implies that the urine of normal individuals would be exceedingly unlikely to change as well.

Adolescent↗
PubMed1985

Citrate and calcium secretion in the pure human pancreatic juice of alcoholic and nonalcoholic men and of chronic pancreatitis patients.

Citrate, calcium and protein have been estimated in pure pancreatic juice after a secretin and a CCK injection in 4 patients presenting with alcoholic calcified pancreatitis (ACP), 10 controls without evidence of pancreatic disease, drinking more than 130 g alcohol/day, and 10 controls without evidence of pancreatic disease, drinking less than 20 g alcohol/day. Citrate is normally secreted in the pancreatic juice and this secretion increases in parallel with protein after CCK injection. Citrate secretion is significantly decreased in the two alcoholic groups. Calcium secretion is increased in the ACP, and reasons are presented to suggest that this may be due to lesions of the ducts. These modifications could play a role in the formation of pancreatic stones which are mostly built up of calcium carbonate.

Alcoholism↗
PubMed1992

Regulation of acute parathyroid hormone release in normal humans: combined calcium and citrate clamp study.

The objective of the present study was to elucidate the dynamics of parathyroid hormone regulation, with particular reference to the mechanism controlling the acute parathyroid hormone release. Through utilization of the citrate clamp technique and the calcium clamp technique we were able, in a standardized way, to stimulate and suppress the parathyroid hormone secretion. Precise bedside measurements of blood ionized calcium and measurements of intact parathyroid hormone were performed. Twelve healthy young volunteers participated in two trials 6-12 wk apart, a citrate clamp (delta-blood ionized calcium -0.19 mmol/l) and a calcium plus citrate clamp (delta-blood ionized calcium +0.22 mmol/l and -0.19 mmol/l). During the citrate clamp, preceded by normal calcemia, serum intact parathyroid hormone peaked to a maximum after 5-10 min, four to six times above baseline concentration and then declined to a steady state two to three times above baseline concentration. During the citrate clamp, preceded by hypercalcemia induced by a calcium clamp, serum intact parathyroid hormone also peaked immediately to about five to nine times above its suppressed level, approximately two times above the baseline concentration. Subsequently, serum intact parathyroid hormone declined to a steady state just below the baseline concentration. In conclusion, within the range studied, the mechanism eliciting the acute serum intact parathyroid hormone release from its depot is a fall in blood ionized calcium, not the absolute concentration of ionized calcium.

Adult↗
PubMed2000

Pharmacokinetic and pharmacodynamic comparison of two calcium supplements in postmenopausal women.

This randomized crossover study compared the single-dose bioavailability and effects on parathyroid function of two commercially formulated calcium supplements containing 500 mg of elemental calcium. Twenty-five postmenopausal women underwent three phases of study wherein they each took a single dose of calcium citrate with a standard breakfast (as Citracal 250 mg + D), calcium carbonate (as Os-Cal 500 mg + D), or placebo at 8 a.m. Blood samples were drawn at baseline and hourly for 4 or 6 hours after each dose. Fasting and postload urine samples were also collected. Compared with calcium carbonate, calcium citrate provided a 46% greater peak-basal variation and 94% higher change in area under the curve for serum calcium and a 41% greater increment in urinary calcium. Moreover, the decrement in serum parathyroid hormone concentration from baseline was greater after calcium citrate. In conclusion, calcium citrate is more bioavailable than calcium carbonate when given with a meal.

Adult↗
PubMed1989

A model system for assessing physicochemical factors affecting calcium absorbability from the intestinal tract.

An in vitro model system was utilized to critically examine physicochemical factors that could play a role in determining the amount of potentially absorbable ionic calcium as well as soluble complexes in the proximal jejunum following ingestion of tricalcium dicitrate, calcium carbonate, or tricalcium diphosphate. The solubility of calcium salts (500 mg calcium each) was tested in 300 ml water containing varying amounts of hydrochloric acid (0, 0.72, 2.4, 7.26, and 24.2 mEq) intended to mimic achlorhydric to peak acid secretory states. Whereas 20% of calcium citrate dissolved in the absence of hydrochloric acid, a negligible amount of calcium carbonate and calcium phosphate underwent dissolution. In solutions containing 0.72-7.26 mEq hydrochloric acid, calcium citrate was more than twofold soluble than calcium carbonate, and calcium phosphate had intermediate solubility. At simulated peak acid secretion, all three salts were completely soluble, or nearly so. To simulate pancreatic bicarbonate secretion, the filtrates obtained from solubility studies were titrated to pH 5, 6, and 7 with sodium hydroxide. Reprecipitation of calcium citrate and calcium carbonate did not occur. However, substantial calcium phosphate reprecipitation took place especially at high pH and in filtrates derived from high hydrochloric acid content. In filtrates derived from reprecipitation experiments (at pH 6 and 7), anionic complexation of calcium was calculated in order to estimate the amount of ionic and complexed calcium. Considerable amount of calcium from dissolved calcium citrate was complexed (60-65%), principally as soluble CaCit-, whereas calcium complexation was negligible in the calcium carbonate and calcium phosphate systems.

Anions↗
PubMed1995

Treatment of postmenopausal osteoporosis with slow-release sodium fluoride. Final report of a randomized controlled trial.

OBJECTIVE: To test whether slow-release sodium fluoride inhibits spinal fractures and is safe to use. DESIGN: Placebo-controlled randomized trial. INTERVENTIONS: Slow-release sodium fluoride, 25 mg twice daily, in four 14-month cycles (12 months receiving sodium fluoride followed by 2 months not receiving it) compared with placebo. Calcium citrate, 400 mg calcium twice daily, continuously in both groups. PATIENTS: 48 of 54 patients who received sodium fluoride and 51 of 56 patients who received placebo completed at least 1 year of the study. All patients had postmenopausal osteoporosis. RESULTS: Compared with the placebo group, the fluoride group had a lower individual vertebral fracture rate (0.064 +/- 0.182 per patient-year compared with 0.205 +/- 0.297 per patient-year; P = 0.002), a higher unadjusted fracture-free rate (85.4% compared with 56.9%; P = 0.001), and a greater survival estimate (relative risk, 0.3 [95% CI, 0.12 to 0.76]) for new fractures. The recurrent spinal fracture rate did not differ between the two groups. The fluoride group had a substantial increase in L2-L4 bone mass of 4% to 5% per year for 4 years, a mean increase in femoral neck bone density of 2.38% +/- 3.33% per year, and no change in radial shaft bone density. The frequency with which minor side effects and appendicular fractures occurred was similar in the two groups; no patients developed microfractures or gastric ulcers. CONCLUSION: Slow-release sodium fluoride and calcium citrate administered for 4 years inhibits new vertebral fractures (but not recurrent fractures), augments spinal and femoral neck bone mass, and is safe to use.

Aged↗
PubMed1990

A controlled trial of the effect of calcium supplementation on bone density in postmenopausal women.

Background. The effectiveness of calcium in retarding bone loss in older postmenopausal women is unclear. Earlier work suggested that the women who were most likely to benefit from calcium supplementation were those with low calcium intakes. Methods. We undertook a double-blind, placebo-controlled, randomized trial to determine the effect of calcium on bone loss from the spine, femoral neck, and radius in 301 healthy postmenopausal women, half of whom had a calcium intake lower than 400 mg per day and half an intake of 400 to 650 mg per day. The women received placebo or either calcium carbonate or calcium citrate malate (500 mg of calcium per day) for two years. Results. In women who had undergone menopause five or fewer years earlier, bone loss from the spine was rapid and was not affected by supplementation with calcium. Among the women who had been postmenopausal for six years or more and who were given placebo, bone loss was less rapid in the group with the higher dietary calcium intake. In those with the lower calcium intake, calcium citrate malate prevented bone loss during the two years of the study; its effect was significantly different from that of placebo (P less than 0.05) at the femoral neck (mean change in bone density [+/- SE], 0.87 +/- 1.01 percent vs. -2.11 +/- 0.93 percent), radius (1.05 +/- 0.75 percent vs. -2.33 +/- 0.72 percent), and spine (-0.38 +/- 0.82 percent vs. -2.85 +/- 0.77 percent). Calcium carbonate maintained bone density at the femoral neck (mean change in bone density, 0.08 +/- 0.98 percent) and radius (0.24 +/- 0.70 percent) but not the spine (-2.54 +/- 0.85 percent). Among the women who had been postmenopausal for six years or more and who had the higher calcium intake, those in all three treatment groups maintained bone density at the hip and radius and lost bone from the spine. Conclusions. Healthy older postmenopausal women with a daily calcium intake of less than 400 mg can significantly reduce bone loss by increasing their calcium intake to 800 mg per day. At the dose we tested, supplementation with calcium citrate malate was more effective than supplementation with calcium carbonate.

Administration, Oral↗
PubMed1999

Calcium bioavailability and parathyroid hormone acute changes after oral intake of dairy and nondairy products in healthy volunteers.

This study was designed to compare calcium bioavailability and serum parathyroid hormone acute changes after oral intake of 500 mg of elemental calcium from liquid milk, yogurt, calcium-citrate-enriched powdered milk or a calcium carbonate pill; or after intake of soybean imitation-milk. After a 12-h fast, blood samples were drawn both at baseline and 1, 2, 3 and 4 h after an oral intake of the above-mentioned products, which were ingested together with a light neutral breakfast. The administration order of the study products was randomly assigned to each of 19 healthy young volunteers (11 females, 8 males). The baseline serum concentrations of ionized calcium, phosphorus and intact parathyroid hormone (iPTH) were normal. Calcium-citrate-enriched powdered milk induced a significant increase in serum ionized calcium (p<0.001) and a significant and continuous decrease in serum iPTH concentration (p<0. 001). Yogurt and the calcium carbonate pill induced a similar but less significant effect, increasing serum ionized calcium (p<0.05) and decreasing serum iPTH (p<0.01). Liquid milk only induced a significant change in serum ionized calcium and iPTH concentration during the first 2 h; this effect was lost during the following 2 h. In conclusion, our study suggests the possibility that the addition of calcium citrate to powered milk may improve calcium bioavailability and enhance the inhibitory effect on serum iPTH in the assayed conditions.

Adult↗
PubMed1991

Calcium supplementation: effect on iron absorption.

The influence of calcium supplements on the absorption of dietary nonheme iron and of iron supplements was evaluated in 61 normal volunteer subjects by use of a double-radioisotope technique. When taken without food, calcium carbonate did not inhibit the absorption of ferrous sulphate with doses of either 300 mg Ca and 37 mg Fe or 600 mg Ca and 18 mg Fe. However, at the latter levels, calcium citrate and calcium phosphate reduced iron absorption significantly by 49% and 62%, respectively. All calcium supplements inhibited absorption of the iron supplement when taken with food. The absorption of dietary nonheme iron was also inhibited by all three supplements. This inhibition was less pronounced from a meal of high iron availability and low calcium content (28%) than from a breakfast meal of low iron availability and high calcium content (55%). These results suggest that taking regular calcium supplements with meals makes it more difficult for women to meet their daily iron requirement.

Absorption↗
PubMed1991

[Combined administration of calcium and citrate reduces urinary oxalate excretion].

Three grams of calcium lactate and 3 g of uralyt U were administered to 39 calcium oxalate stone formers. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The mechanism of action of these drugs and the diet which might produce a similar effect were discussed.

Adult↗
PubMed1979

Inorganic constituents of milk: I. Correlation of soluble calcium with citrate in bovine milk.

A high correlation was found between soluble calcium and citrate concentrations during a study of seasonal changes in the composition of the commercial milk supply to South-west Scotland. A simple physicochemical model of the ion equilibria in the aqueous phase of milk suggests that the observed correlation is causal. This hypothesis was corroborated by an analysis of data on individual cow milks and by experiments involving the addition of citrate to milk at constant pH.

Animals↗
PubMed1984

An evaluation of the importance of gastric acid secretion in the absorption of dietary calcium.

Since calcium solubility is a prerequisite to calcium absorption, and since solubility of calcium is highly pH-dependent, it has been generally assumed that gastric acid secretion and gastric acidity play an important role in the intestinal absorption of calcium from ingested food or calcium salts such as CaCO3. To evaluate this hypothesis, we developed a method wherein net gastrointestinal absorption of calcium can be measured after ingestion of a single meal. A large dose of cimetidine, which markedly reduced gastric acid secretion, had no effect on calcium absorption in normal subjects, and an achlorhydric patient with pernicious anemia absorbed calcium normally. This was true regardless of the major source of dietary calcium (i.e., milk, insoluble calcium carbonate, or soluble calcium citrate). Moreover, calcium absorption after CaCO3 ingestion was the same when intragastric contents were maintained at pH 7.4 (by in vivo titration) as when intragastric pH was 3.0. On the basis of these results, we conclude that gastric acid secretion and gastric acidity do not normally play a role in the absorption of dietary calcium. Other possible mechanisms by which the gastrointestinal tract might solubilize ingested calcium complexes and salts are discussed.

Achlorhydria↗
PubMed1990

Effect of calcium citrate-malate on skeletal development in young, growing rats.

It has been previously demonstrated that calcium from calcium citrate-malate (CCM), a mixture of calcium, citric acid and malic acid, is better-absorbed than calcium from calcium carbonate (CaCO3) in humans and in rats. It was of interest to determine if this differential in absorption would result in differences in bone development under chronic feeding conditions. The present study was designed to compare CCM with CaCO3 for effects on bone development in weanling female C/D rats fed either CCM or CaCO3 at 0.3 or 0.6% dietary Ca for 4 or 12 wk. There was a nonsignificant trend for rats fed CCM to weigh more and have larger bones than rats fed CaCO3. Histologic evaluation of cortical and trabecular bone revealed normal bone formation in all rats. Trabecular bone was significantly affected by calcium level and source. The 0.3% Ca diets (either source) resulted in reduced trabecular bone volumes in tibias. After 4 wk, rats fed CCM had 23-25% more trabecular bone than rats fed CaCO3. By 12 wk, the difference was even greater; rats fed CCM had 44-47% more trabecular bone than rats fed CaCO3. Dietary calcium source did not affect cortical bone. It is concluded that because of its positive effects on bone, CCM is a more bioavailable calcium source than CaCO3.

Animals↗
PubMed1979

[Changes in ionized calcium and citrate levels in dogs during mechanical autotransfusion with heparin, ACD and CPD].

The control of ionized calcium (Ca++), total calcium, and citrate levels in serum were determined in dogs during autotransfusion (AT) of blood stabilized with heparin, ACD (formula B) and CPD. Blood samples were taken according to the changes of aortic pressure (AOP), which was continuously monitored. Taking the values during the stable phase of AOP preceding the AT as baseline, Ca++ dropped by 27% with ACD and by 34% with CPD at the maximum decrease of AOP immediately after the AT. The corresponding increase of citrate was 174% with ACD and 521% with CPD, while total calcium remained stable. Thus cardiac depression after AT of citrated blood seems to be mainly caused by the drop of Ca++, which is significantly more pronounced with CPD, corresponding to the higher content of citrate.

Animals↗
PubMed1989

[Calcium and citrate excretion by patients with calculi and healthy probands during induced acidosis].

Acidosis induced increase in renal calcium excretion and decrease in renal citrate excretion was produced by means of ammonium chloride load in 15 patients with recurrent oxalate lithiasis and in 15 control subjects. The expected increase in the calcium citrate relationship in urine is more marked and more lasting in stone patients. Stone formers obviously respond to an acidotic metabolic situation by a more clear relative decrease in citrate excretion, in addition to more intensive calcium excretion, which is known. A certain individual sensitivity of renal tubular mechanisms is discussed with regard to acid base changes.

Acid-Base Equilibrium↗
PubMed1997

Evaluation of the calcium-PTH axis and renal handling of phosphate by calcium and citrate clamp techniques in normal subjects and in patients with heavy proteinuria.

We studied the effect of induced hyper- and hypocalcemia on parathyroid function and renal handling of phosphate in healthy subjects (n = 10) and in patients with heavy proteinuria, mean 5.6 +/- 1.9 g/24 hours (n = 5). We used calcium and citrate clamp techniques. Hypercalcemia was rapidly induced by calcium infusion and maintained for 120 min, and correspondingly, hypocalcemia by citrate infusion. The suppression of intact PTH secretion during calcium clamp was similar (to the level of < or = 0.8 pmol/l) in both groups. The response of the parathyroid glands to hypocalcemia was similar in normal subjects and proteinuric patients. Both groups showed a peak of PTH secretion at 10 min, 18.9 +/- 6.7 pmol/l in healthy subjects and 20.4 +/- 7.4 pmol/l in patients. The peak levels were 4.8-7.2 times and 4.0-6.7 times the baseline level, respectively. Thereafter the plasma PTH concentration declined to a fairly constant steady-state level (twice the baseline level) in spite of maintained hypocalcemia. The area under the curve of the plasma concentrations of intact PTH at various times (AUC0-120) was 890 +/- 324 pmol/l/min in normal subjects and 989 +/- 331 pmol/l/min in proteinuric patients, the difference between the groups being again not significant. The renal threshold phosphate concentration (TmPO4/GFR) increased during calcium infusion and decreased during citrate infusion in both groups. During recovery from hypocalcemia PTH levels were lower than during hypocalcemic induction at corresponding serum calcium levels. Using calcium and citrate clamp techniques, we found that the response of the parathyroid glands in acute and maintained hypercalcemia and hypocalcemia, and renal phosphate handling in patients with heavy proteinuria was not different from that of healthy subjects.

Adult↗